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Amyotrophic lateral sclerosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohsen Basiri M.D.

Overview

Overview

Amyotrophic Lateral Sclerosis is a chronic progressive neurological disease that affects both upper and lower motor neurons. It presents with muscle spasms, fasciculation, weakness and which could ultimately lead to muscles paralysis. ALS is diagnosed clinically, however additional testing with electromyography to confirm muscle denervation. Laboratory tests might be required to rule out other reversible causes of weakness. ALS has a poor prognosis with death usually due to respiratory complications with a median survival of 3-5 years. ALS is managed by a multidisciplinary care setting with fewer disease modifying agents to date.

Historical Perspective

Historical Perspective

Amyotrophic Lateral Sclerosis was first described by French neurologist Jean-Martin Charcot in his Tuesday lectures in late 1860 and then a publication in 1874. He is also known as the Father of Amyotrophic Lateral Sclerosis because of his devotion to the disease. He complied 50 years of previous work on muscle weakness. He was the first scientist to link the disease to its specific pathology. [1]

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2]Mohamadmostafa Jahansouz M.D.[3]

Overview

ALS is classified into two sub-groups: Familial ALS and Sporadic ALS.

Classification

  • Familial ALS accounts for approximately 5%-10% of all ALS cases and is caused due to genetic factors.
  • Sporadic ALS accounts for the remaining 90%-95% of ALS with no known cause.


[1]

References

  1. ↑ Hulisz D (2018). “Amyotrophic lateral sclerosis: disease state overview”. Am J Manag Care. 24 (15 Suppl): S320–S326. PMID 30207670.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

A possible explanation of Amyotrophic lateral Sclerosis pathophysiology must include processes involved in the development of both Familial and Sporadic forms of ALS. The most commonly accepted view suggests that the disorder is the likely result of a complex interplay between genetic and environmental factors. Other theories also suggest that the pathogenesis of ALS is a multistep process. In the Case of Familial ALS pathological genes causing disease are present from birth however accumulation of disease-causing proteins might take time to build up and exposure to environmental toxins might trigger the multistep process. However, in most cases, Amyotrophic lateral Sclerosis is a Sporadic form in which a small impact of genetic factors with a major contribution from environmental factors. Therefore, the most common explanation for ALS pathophysiology is a two-step process of exposure to genetic risk factors and environmental triggers that triggers the downstream cascade pathway. [1]

Pathophysiology

Pathological Features

The central pathological feature involving Amyotrophic lateral sclerosis is the death of the motor neurons in the motor cortex, the brain stem, and the spinal cord. Pathological neuronal degeneration in the corticospinal tracts leads to thinning and sclerosis of the neuronal tracts. As more neurons die patients with amyotrophic lateral sclerosis experiences symptoms of denervation atrophy of the limbs, and swallowing, speech process becomes difficult with disease progression. The degeneration process of motor neurons is also associated with neuronal inflammation that also leads to the proliferation of supporting cells- astroglial, microglia, and oligodendrocytes. [2] The majority of the cases of ALS are sporadic however familial cases account for 5-10% of ALS. Several genes mutations are linked to the pathogenesis of Familial cases of ALS that includes SOD1 (superoxide dismutase), TAR DNA binding protein (TDP-43), and Fused in Sarcoma (FUS) also known as Translocated in Sarcoma (TLS) accounts for almost 30% of cases. Mutations in several other genes can also lead to ALS/ALS-like syndrome. While causes of most of the sporadic ALS and familial ALS are not known yet. However fronto-temporal lobar dementia may occur in some cases of ALS syndrome. Mutations in UBQLN2 encodes for ubiquitin-like proteins ubiquilin-2 which regulates degradation of ubiquitinated proteins. Mutations in UBQLN2 leads to defects in the protein degradation pathway and abnormal protein aggregated which ultimately causes neurodegeneration that accounts for ALS and dementia pathway. [3]

References

  1. ↑ Al-Chalabi A, Calvo A, Chio A, Colville S, Ellis CM, Hardiman O; et al. (2014). “Analysis of amyotrophic lateral sclerosis as a multistep process: a population-based modelling study”. Lancet Neurol. 13 (11): 1108–1113. doi:10.1016/S1474-4422(14)70219-4. PMC 4197338. PMID 25300936.
  2. ↑ Brown RH, Al-Chalabi A (2017). “Amyotrophic Lateral Sclerosis”. N Engl J Med. 377 (2): 162–172. doi:10.1056/NEJMra1603471. PMID 28700839.
  3. ↑ Deng, Han-Xiang; Chen, Wenjie; Hong, Seong-Tshool; Boycott, Kym M.; Gorrie, George H.; Siddique, Nailah; Yang, Yi; Fecto, Faisal; Shi, Yong; Zhai, Hong; Jiang, Hujun; Hirano, Makito; Rampersaud, Evadnie; Jansen, Gerard H.; Donkervoort, Sandra; Bigio, Eileen H.; Brooks, Benjamin R.; Ajroud, Kaouther; Sufit, Robert L.; Haines, Jonathan L.; Mugnaini, Enrico; Pericak-Vance, Margaret A.; Siddique, Teepu (2011). “Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia”. Nature. 477 (7363): 211–215. doi:10.1038/nature10353. ISSN 0028-0836.

References

Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

Approximately 5-10% of cases of ALS are familial ALS. More than 25 different genes could be linked to the causation of familial ALS. However, the remaining majority 90-95% of ALS cases are Sporadic ALS. There is no known cause for Sporadic ALS.

Cause

Approximately 5-10% of Familial ALS cases could be linked to different genes and their pathological pathways. More than 25 different genes mutations are attributed to Familial ALS. The most common ones include:

[1]

References

  1. ↑ Källstig E, McCabe BD, Schneider BL (2021). “The Links between ALS and NF-κB”. Int J Mol Sci. 22 (8). doi:10.3390/ijms22083875. PMC 8070122 Check |pmc= value (help). PMID 33918092 PMID: 33918092 Check |pmid= value (help).

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Differentiating Amyotrophic lateral sclerosis from other Diseases

Differentiating Amyotrophic lateral sclerosis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]Tarek Nafee, M.D. [3]

Overview

Amyotrophic lateral sclerosis is a neurodegenerative disease of upper and lower motor neurons. It is diagnosed clinically along with supportive electrophysiological testing. However, there is no specific biological marker that correlates with the disease pathology. The clinical diagnosis is straightforward in the majority of the cases, but false positive and false negative cases can arise early in the disease process. It usually occurs when only upper motor neurons or lower motor neurons signs and symptoms are present. It might be difficult to exclude ALS with only LMN signs with other spinal muscular atrophies, poliomyelitis, and Kennedy disease, etc.

[1]

Differential Diagnosis

  • PPS presents with focal muscle weakness that very slowly progresses to other muscle groups over many years, and does not usually cause death. Patients who present with chronic respiratory muscle weakness should have a thorough evaluation to rule out ALS, as the onset of these symptoms are found in about 3% of ALS patients.[5][4]
Diseases History and Physical Diagnostic tests Other Findings
Motor Deficit Sensory deficit Cranial nerve Involvement Autonomic dysfunction Proximal/Distal/Generalized Ascending/Descending/Systemic Unilateral (UL)

or Bilateral (BL)

or

No Lateralization (NL)

Onset Lab or Imaging Findings Specific test
Adult Botulism + – + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis
Infant Botulism + – + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Flaccid paralysis (Floppy baby syndrome), possible respiratory paralysis
Guillian-Barre syndrome[6] + – – – Generalized Ascending BL Insidious CSF: ↑Protein

↓Cells

Clinical & Lumbar Puncture Progressive ascending paralysis following infection, possible respiratory paralysis
Eaton Lambert syndrome[7] + – + + Generalized Systemic BL Intermittent EMG, repetitive nerve stimulation test (RNS) Voltage gated calcium channel (VGCC) antibody Diplopia, ptosis, improves with movement (as the day progresses)
Myasthenia gravis[8] + – + + Generalized Systemic BL Intermittent EMG, Edrophonium test Ach receptor antibody Diplopia, ptosis, worsening with movement (as the day progresses)
Electrolyte disturbance[9] + + – – Generalized Systemic BL Insidious Electrolyte panel ↓Ca++, ↓Mg++, ↓K+ Possible arrhythmia
Organophosphate toxicity[10] + + – + Generalized Ascending BL Sudden Clinical diagnosis: physical exam & history Clinical suspicion confirmed with RBC AchE activity History of exposure to insecticide or living in farming environment. with : Diarrhea, Urination, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating
Tick paralysis (Dermacentor tick)[11] + – – – Generalized Ascending BL Insidious Clinical diagnosis: physical exam & history – History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
Tetrodotoxin poisoning[12] + – + + Generalized Systemic BL Sudden Clinical diagnosis: physical exam & dietary history – History of consumption of puffer fish species.
Stroke[13] +/- +/- +/- +/- Generalized Systemic UL Sudden MRI +ve for ischemia or hemorrhage MRI Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation.
Poliomyelitis[14] + + + +/- Proximal > Distal Systemic BL or UL Sudden PCR of CSF Asymmetric paralysis following a flu-like syndrome.
Transverse myelitis[15] + + + + Proximal > Distal Systemic BL or UL Sudden MRI & Lumbar puncture MRI History of chronic viral or autoimmune disease (e.g. HIV)
Neurosyphilis[16][17] + + – +/- Generalized Systemic BL Insidious MRI & Lumbar puncture CSF VDRL-specifc

CSF FTA-Ab -sensitive[18]

History of unprotected sex or multiple sexual partners.

History of genital ulcer (chancre), diffuse maculopapular rash.

Muscular dystrophy[19] + – – – Proximal > Distal Systemic BL Insidious Genetic testing Muscle biopsy Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. Gower sign positive.
Multiple sclerosis exacerbation[20] + + + + Generalized Systemic NL Sudden ↑CSF IgG levels

(monoclonal)

Clinical assessment and MRI [21] Blurry vision, urinary incontinence, fatigue
Amyotrophic lateral sclerosis[22] + – – – Generalized Systemic BL Insidious Normal LP (to rule out DDx) MRI & LP Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity).
Inflammatory myopathy[23] + – – – Proximal > Distal Systemic UL or BL Insidious Elevated CK & Aldolase Muscle biopsy Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.

References

  1. ↑ Pradat PF, Bruneteau G (2006). “[Differential diagnosis and atypical subsets of amyotrophic lateral sclerosis]”. Rev Neurol (Paris). 162 Spec No 2: 4S81–4S90. PMID 17128093.
  2. ↑ Pinto S, Swash M, de Carvalho M (2014). “Does surgery accelerate progression of amyotrophic lateral sclerosis?”. J Neurol Neurosurg Psychiatry. 85 (6): 643–6. doi:10.1136/jnnp-2013-305770. PMID 23922387.
  3. ↑ 3.0 3.1 Hardiman O, van den Berg LH, Kiernan MC (2011). “Clinical diagnosis and management of amyotrophic lateral sclerosis”. Nat Rev Neurol. 7 (11): 639–49. doi:10.1038/nrneurol.2011.153. PMID 21989247.
  4. ↑ 4.0 4.1 4.2 Zarei S, Carr K, Reiley L, Diaz K, Guerra O, Altamirano PF; et al. (2015). “A comprehensive review of amyotrophic lateral sclerosis”. Surg Neurol Int. 6: 171. doi:10.4103/2152-7806.169561. PMC 4653353. PMID 26629397.
  5. ↑ Pfeffer G, Povitz M, Gibson GJ, Chinnery PF (2015). “Diagnosis of muscle diseases presenting with early respiratory failure”. J Neurol. 262 (5): 1101–14. doi:10.1007/s00415-014-7526-1. PMID 25377282.
  6. ↑ Talukder RK, Sutradhar SR, Rahman KM, Uddin MJ, Akhter H (2011). “Guillian-Barre syndrome”. Mymensingh Med J. 20 (4): 748–56. PMID 22081202.
  7. ↑ Merino-Ramírez MÁ, Bolton CF (2016). “Review of the Diagnostic Challenges of Lambert-Eaton Syndrome Revealed Through Three Case Reports”. Can J Neurol Sci. 43 (5): 635–47. doi:10.1017/cjn.2016.268. PMID 27412406.
  8. ↑ Gilhus NE (2016). “Myasthenia Gravis”. N Engl J Med. 375 (26): 2570–2581. doi:10.1056/NEJMra1602678. PMID 28029925.
  9. ↑ Ozono K (2016). “[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]”. Clin Calcium. 26 (2): 215–22. doi:CliCa1602215222 Check |doi= value (help). PMID 26813501.
  10. ↑ Kamanyire R, Karalliedde L (2004). “Organophosphate toxicity and occupational exposure”. Occup Med (Lond). 54 (2): 69–75. PMID 15020723.
  11. ↑ Pecina CA (2012). “Tick paralysis”. Semin Neurol. 32 (5): 531–2. doi:10.1055/s-0033-1334474. PMID 23677663.
  12. ↑ Bane V, Lehane M, Dikshit M, O’Riordan A, Furey A (2014). “Tetrodotoxin: chemistry, toxicity, source, distribution and detection”. Toxins (Basel). 6 (2): 693–755. doi:10.3390/toxins6020693. PMC 3942760. PMID 24566728.
  13. ↑ Kuntzer T, Hirt L, Bogousslavsky J (1996). “[Neuromuscular involvement and cerebrovascular accidents]”. Rev Med Suisse Romande. 116 (8): 605–9. PMID 8848683.
  14. ↑ Laffont I, Julia M, Tiffreau V, Yelnik A, Herisson C, Pelissier J (2010). “Aging and sequelae of poliomyelitis”. Ann Phys Rehabil Med. 53 (1): 24–33. doi:10.1016/j.rehab.2009.10.002. PMID 19944665.
  15. ↑ West TW (2013). “Transverse myelitis–a review of the presentation, diagnosis, and initial management”. Discov Med. 16 (88): 167–77. PMID 24099672.
  16. ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
  17. ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  18. ↑ Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
  19. ↑ Falzarano MS, Scotton C, Passarelli C, Ferlini A (2015). “Duchenne Muscular Dystrophy: From Diagnosis to Therapy”. Molecules. 20 (10): 18168–84. doi:10.3390/molecules201018168. PMID 26457695.
  20. ↑ Filippi M, Preziosa P, Rocca MA (2016). “Multiple sclerosis”. Handb Clin Neurol. 135: 399–423. doi:10.1016/B978-0-444-53485-9.00020-9. PMID 27432676.
  21. ↑ Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). “Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group”. Arch Neurol. 51 (1): 61–6. PMID 8274111.
  22. ↑ Riva N, Agosta F, Lunetta C, Filippi M, Quattrini A (2016). “Recent advances in amyotrophic lateral sclerosis”. J Neurol. 263 (6): 1241–54. doi:10.1007/s00415-016-8091-6. PMC 4893385. PMID 27025851.
  23. ↑ Michelle EH, Mammen AL (2015). “Myositis Mimics”. Curr Rheumatol Rep. 17 (10): 63. doi:10.1007/s11926-015-0541-0. PMID 26290112.
Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

The incidence and prevalence of ALS are rising globally. More resources should be dedicated to the advancement of care and research of ALS.

Epidemiology and Demographics

Incidence

  • The incidence of ALS is around 0.6-3.8 per 100000 person-years.

Prevalance

The prevalence of ALS is between 4.1-8.4 per 100000 person-years.

Age Onset

The median age of onset of ALS is between 51-66 years.

Gender

The male population is more commonly affected by ALS than females.

[1]

References

  1. ↑ Longinetti E, Fang F (2019). “Epidemiology of amyotrophic lateral sclerosis: an update of recent literature”. Curr Opin Neurol. 32 (5): 771–776. doi:10.1097/WCO.0000000000000730. PMC 6735526 Check |pmc= value (help). PMID 31361627.


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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

Common risk factors in the development and progression of amyotrophic lateral sclerosis largely remain unknown. Other common risk factors associated include: Age, Smoking, oxidative stress.

Risk Factors

Common Risk Factors

  • Common risk factors in the development of [Amyotrophic lateral sclerosis] include:
    • Smoking
      • Cigarette smoke might be considered an established risk factor for Sporadic Amyotrophic lateral sclerosis (level A rating, 3 class II studies, 1 class III study).[1]
    • Chemical exposure
      • ALS has shown an association with exposure to agricultural chemicals such as pesticides, fertilizers, herbicides, insecticides, and formaldehyde.[2]
      • Among all the heavy metals that might be associated with ALS, lead exposure seems to be studied the most possibly due to the ALS-like symptoms experienced by people exposed to high concentrations of lead.[3]
    • Radiation
    • Diet
    • Genetic causes[6]

References

  1. ↑ Armon C (2009). “Smoking may be considered an established risk factor for sporadic ALS”. Neurology. 73 (20): 1693–8. doi:10.1212/WNL.0b013e3181c1df48. PMC 2788806. PMID 19917993.
  2. ↑ Welty DF, Schielke GP, Rothstein JD (1995). “Potential treatment of amyotrophic lateral sclerosis with gabapentin: a hypothesis”. Ann Pharmacother. 29 (11): 1164–7. doi:10.1177/106002809502901118. PMID 8573965.
  3. ↑ Kamel F, Umbach DM, Munsat TL, Shefner JM, Hu H, Sandler DP (2002). “Lead exposure and amyotrophic lateral sclerosis”. Epidemiology. 13 (3): 311–9. PMID 11964933.
  4. ↑ Morozova N, Weisskopf MG, McCullough ML, Munger KL, Calle EE, Thun MJ; et al. (2008). “Diet and amyotrophic lateral sclerosis”. Epidemiology. 19 (2): 324–37. doi:10.1097/EDE.0b013e3181632c5d. PMID 18300717.
  5. ↑ Veldink JH, Kalmijn S, Groeneveld GJ, Wunderink W, Koster A, de Vries JH; et al. (2007). “Intake of polyunsaturated fatty acids and vitamin E reduces the risk of developing amyotrophic lateral sclerosis”. J Neurol Neurosurg Psychiatry. 78 (4): 367–71. doi:10.1136/jnnp.2005.083378. PMC 2077791. PMID 16648143.
  6. ↑ Deivasigamani S, Verma HK, Ueda R, Ratnaparkhi A, Ratnaparkhi GS (2014). “A genetic screen identifies Tor as an interactor of VAPB in a Drosophila model of amyotrophic lateral sclerosis”. Biol Open. 3 (11): 1127–38. doi:10.1242/bio.201410066. PMC 4232771. PMID 25361581.

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

There is insufficient evidence to recommend routine screening for Amyotrophic lateral sclerosis.

Screening

There is insufficient evidence to recommend routine screening for Amyotrophic lateral sclerosis.


References

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

The prognosis of Amyotrophic lateral sclerosis is generally poor with the majority of patients dying within 3-5 years of diagnosis.

Natural History, Complications, and Prognosis

Natural History

  • The symptoms of Amyotrophic lateral sclerosis usually develop in the fifth decade of life.[1][2]
  • Only 5% of the cases have an onset <30 years of age.[1][2]

Complications

  • With the progression of ALS, patients develop the distinctive feature of a combination of UMN and LMN degeneration signs within the same CNS region.

Prognosis

  • Prognosis is generally poor, and the 30 months survival rate of patients with ALS is approximately 5%.[3]
  • Only 20% of the patients survive between 5 and 10 years after symptoms onset.[3]
  • Reduced survival to the disease is related to the older age of symptom onset, early respiratory muscle dysfunction, and bulbar onset disease. On the other hand, limb-onset disease, younger age at presentation of the disease and longer diagnostic delay are independent predictors of prolonged survival.[4]

Some ALS subtypes vary according to prognosis. LMN form of ALS, which includes flail-limb variant and PMA, shows a slower progression than other forms of ALS. A prognosis of 2–4 years is seen in the pure bulbar palsy phenotype, which usually affects women older than 65 years of age. In this type of ALS, the disease remains localized to the oropharyngeal musculature and UMN features predominate.[5]

References

  1. ↑ 1.0 1.1 Logroscino G, Traynor BJ, Hardiman O, Chio’ A, Couratier P, Mitchell JD; et al. (2008). “Descriptive epidemiology of amyotrophic lateral sclerosis: new evidence and unsolved issues”. J Neurol Neurosurg Psychiatry. 79 (1): 6–11. doi:10.1136/jnnp.2006.104828. PMID 18079297.
  2. ↑ 2.0 2.1 2.2 Zarei S, Carr K, Reiley L, Diaz K, Guerra O, Altamirano PF; et al. (2015). “A comprehensive review of amyotrophic lateral sclerosis”. Surg Neurol Int. 6: 171. doi:10.4103/2152-7806.169561. PMC 4653353. PMID 26629397.
  3. ↑ 3.0 3.1 Talbot K (2009). “Motor neuron disease: the bare essentials”. Pract Neurol. 9 (5): 303–9. doi:10.1136/jnnp.2009.188151. PMID 19762894.
  4. ↑ Vucic S, Kiernan MC (2007). “Abnormalities in cortical and peripheral excitability in flail arm variant amyotrophic lateral sclerosis”. J Neurol Neurosurg Psychiatry. 78 (8): 849–52. doi:10.1136/jnnp.2006.105056. PMC 2117729. PMID 17210625.
  5. ↑ Sanjak M, Konopacki R, Capasso R, Roelke KA, Peper SM, Houdek AM; et al. (2004). “Dissociation between mechanical and myoelectrical manifestation of muscle fatigue in amyotrophic lateral sclerosis”. Amyotroph Lateral Scler Other Motor Neuron Disord. 5 (1): 26–32. doi:10.1080/14660820310017551. PMID 15204021.

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Diagnosis

Diagnosis

Diagnostic Evaluation | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters
References

References

  1. ↑ Katz JS, Dimachkie MM, Barohn RJ (2015). “Amyotrophic Lateral Sclerosis: A Historical Perspective”. Neurol Clin. 33 (4): 727–34. doi:10.1016/j.ncl.2015.07.013. PMID 26515617.

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